PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34894066-2 2022 Imatinib, a receptor tyrosine kinase (RTK) inhibitor, has been used in Penttinen syndrome (PS) patients with good results. Imatinib Mesylate 0-8 ret proto-oncogene Homo sapiens 12-36 34894066-2 2022 Imatinib, a receptor tyrosine kinase (RTK) inhibitor, has been used in Penttinen syndrome (PS) patients with good results. Imatinib Mesylate 0-8 ret proto-oncogene Homo sapiens 38-41 26098203-3 2015 Despite the successful clinical use of imatinib mesylate, a selective receptor tyrosine kinase (RTK) inhibitor that targets KIT, PDGFRA and BCR-ABL, we still do not have treatment for the long-term control of advanced GIST. Imatinib Mesylate 39-56 ret proto-oncogene Homo sapiens 70-94 29697413-2 2018 Our present data show that BGJ398, a selective fibroblast growth factor receptor (FGFR) inhibitor, sensitizes imatinib (IM)-resistant GIST cells with receptor tyrosine kinase (RTK) switch (loss of c-KIT/gain of pFGFR2a) to the low doses of topoisomerase II inhibitors - doxorubicin (Dox) and etoposide (Eto). Imatinib Mesylate 110-118 ret proto-oncogene Homo sapiens 150-174 29697413-2 2018 Our present data show that BGJ398, a selective fibroblast growth factor receptor (FGFR) inhibitor, sensitizes imatinib (IM)-resistant GIST cells with receptor tyrosine kinase (RTK) switch (loss of c-KIT/gain of pFGFR2a) to the low doses of topoisomerase II inhibitors - doxorubicin (Dox) and etoposide (Eto). Imatinib Mesylate 110-118 ret proto-oncogene Homo sapiens 176-179 28768491-2 2017 These GISTs generally respond well to therapy with the RTK inhibitor imatinib mesylate (IM), although initial response is genotype-dependent. Imatinib Mesylate 69-86 ret proto-oncogene Homo sapiens 55-58 28768491-2 2017 These GISTs generally respond well to therapy with the RTK inhibitor imatinib mesylate (IM), although initial response is genotype-dependent. Imatinib Mesylate 88-90 ret proto-oncogene Homo sapiens 55-58 34944663-8 2021 Based on this finding, we tested the efficacy of hydrazostat in combination with RTK inhibitor imatinib. Imatinib Mesylate 95-103 ret proto-oncogene Homo sapiens 81-84 34203261-2 2021 Here, we show that the receptor tyrosine kinase inhibitor imatinib (also known as STI571, Gleevec) can inhibit the expression of the endogenous ACE2 gene at both the transcript and protein levels. Imatinib Mesylate 58-66 ret proto-oncogene Homo sapiens 23-47 33066449-3 2020 The clinical use of the RTK inhibitor imatinib has significantly improved the management of GIST patients; however, imatinib resistance remains a challenge. Imatinib Mesylate 38-46 ret proto-oncogene Homo sapiens 24-27 28915580-6 2017 In line with these clinical evidences computer simulations, biophysical techniques and in vitro experiments demonstrated that the receptor tyrosine kinase KIT carrying the Delta574-580 mutation displays constitutive phosphorylation, which can be switched-off upon Imatinib treatment. Imatinib Mesylate 264-272 ret proto-oncogene Homo sapiens 130-154 26026391-7 2015 Some mice were given the RTK inhibitor imatinib after injection of cancer cells; tumor growth was measured based on bioluminescence. Imatinib Mesylate 39-47 ret proto-oncogene Homo sapiens 25-28 26098203-3 2015 Despite the successful clinical use of imatinib mesylate, a selective receptor tyrosine kinase (RTK) inhibitor that targets KIT, PDGFRA and BCR-ABL, we still do not have treatment for the long-term control of advanced GIST. Imatinib Mesylate 39-56 ret proto-oncogene Homo sapiens 96-99 22286373-3 2012 Some clinical trials have been conducted showing the ability of targeted therapies able to inhibit RET(sorafenib, imatinib, vandetanib) in stabilizing the course of the disease. Imatinib Mesylate 114-122 ret proto-oncogene Homo sapiens 99-102 30349606-6 2013 Motesanib, sorafenib, vandetanib, sunitinib, lenvatinib, imatinib and cabozantinib are multi-kinase inhibitors that have the ability of inhibiting the rearranged during transection (RET) and vascular endothelial growth factor receptor (VEGFR), and other kinases, and have been used in advanced differentiated thyroid carcinoma. Imatinib Mesylate 57-65 ret proto-oncogene Homo sapiens 182-185 15548358-1 2004 The platelet-derived growth factor receptor (PDGFR) is a receptor tyrosine kinase overexpressed in a subset of solid tumors and therefore is the target of drugs inhibiting this function such as imatinib mesylate (Gleevec). Imatinib Mesylate 194-211 ret proto-oncogene Homo sapiens 57-81 16782438-0 2006 Cellular effects of imatinib on medullary thyroid cancer cells harboring multiple endocrine neoplasia Type 2A and 2B associated RET mutations. Imatinib Mesylate 20-28 ret proto-oncogene Homo sapiens 128-131 16782438-6 2006 RESULTS: Imatinib inhibited RET Y1062 phosphorylation in a dose-dependent manner after 1.5 hours of exposure. Imatinib Mesylate 9-17 ret proto-oncogene Homo sapiens 28-31 16782438-11 2006 CONCLUSIONS: Imatinib inhibits RET-mediated MTC cell growth affecting RET protein levels in vitro in a dose-dependent manner. Imatinib Mesylate 13-21 ret proto-oncogene Homo sapiens 31-34 16782438-11 2006 CONCLUSIONS: Imatinib inhibits RET-mediated MTC cell growth affecting RET protein levels in vitro in a dose-dependent manner. Imatinib Mesylate 13-21 ret proto-oncogene Homo sapiens 70-73 16782438-12 2006 The concentration of imatinib necessary to inhibit RET in vitro, however, makes it impossible to conclude that imatinib monotherapy will be a good option for systemic therapy of MTC. Imatinib Mesylate 21-29 ret proto-oncogene Homo sapiens 51-54 17064855-3 2006 Elucidation of the aberrant receptor tyrosine kinase (RTK) model of GIST pathogenesis through mutations in c-kit and platelet-derived growth factor alpha PDGFRalpha proto-oncogenes has been prerequisite to the use of imatinib mesylate (STI571, Gleevec; Novartis, Switzerland), a molecular inhibitor of several tyrosine kinases, in the treatment of GISTs. Imatinib Mesylate 217-234 ret proto-oncogene Homo sapiens 28-52 17064855-3 2006 Elucidation of the aberrant receptor tyrosine kinase (RTK) model of GIST pathogenesis through mutations in c-kit and platelet-derived growth factor alpha PDGFRalpha proto-oncogenes has been prerequisite to the use of imatinib mesylate (STI571, Gleevec; Novartis, Switzerland), a molecular inhibitor of several tyrosine kinases, in the treatment of GISTs. Imatinib Mesylate 217-234 ret proto-oncogene Homo sapiens 54-57 15922853-1 2005 Receptor tyrosine kinase (RTK) targeted agents such as trastuzumab, imatinib, bevacizumab, and gefitinib inhibitors have illustrated the utility of targeting this protein class for treatment of selected cancers. Imatinib Mesylate 68-76 ret proto-oncogene Homo sapiens 0-24 15922853-1 2005 Receptor tyrosine kinase (RTK) targeted agents such as trastuzumab, imatinib, bevacizumab, and gefitinib inhibitors have illustrated the utility of targeting this protein class for treatment of selected cancers. Imatinib Mesylate 68-76 ret proto-oncogene Homo sapiens 26-29 19900123-2 2010 The receptor tyrosine kinase (RTK) inhibitor imatinib mesylate has been approved as the first-line choice of therapy for this group of patients, while the RTK inhibitor, sunitinib malate, has been approved for the treatment of GIST after disease progression or intolerance to imatinib. Imatinib Mesylate 45-62 ret proto-oncogene Homo sapiens 4-28 19900123-2 2010 The receptor tyrosine kinase (RTK) inhibitor imatinib mesylate has been approved as the first-line choice of therapy for this group of patients, while the RTK inhibitor, sunitinib malate, has been approved for the treatment of GIST after disease progression or intolerance to imatinib. Imatinib Mesylate 45-62 ret proto-oncogene Homo sapiens 30-33 19900123-2 2010 The receptor tyrosine kinase (RTK) inhibitor imatinib mesylate has been approved as the first-line choice of therapy for this group of patients, while the RTK inhibitor, sunitinib malate, has been approved for the treatment of GIST after disease progression or intolerance to imatinib. Imatinib Mesylate 45-53 ret proto-oncogene Homo sapiens 4-28 19900123-2 2010 The receptor tyrosine kinase (RTK) inhibitor imatinib mesylate has been approved as the first-line choice of therapy for this group of patients, while the RTK inhibitor, sunitinib malate, has been approved for the treatment of GIST after disease progression or intolerance to imatinib. Imatinib Mesylate 45-53 ret proto-oncogene Homo sapiens 30-33 18314611-2 2007 One very effective tyrosine kinase inhibitor is imatinib mesylate inhibiting the KIT receptor tyrosine kinase in gastrointestinal stromal tumors (GISTs) which often carry activating mutations in the KIT gene. Imatinib Mesylate 48-65 ret proto-oncogene Homo sapiens 85-109 16401709-1 2006 The introduction of imatinib, an orally administered inhibitor of the KIT receptor tyrosine kinase, is prompting revision of the management algorithms that have traditionally guided the treatment of gastrointestinal stromal tumor (GIST). Imatinib Mesylate 20-28 ret proto-oncogene Homo sapiens 74-98 15709206-4 2005 Treatment with STI571 resulted in inhibition of RET phosphorylation, cell proliferation, tumor growth and invasiveness. Imatinib Mesylate 15-21 ret proto-oncogene Homo sapiens 48-51 15548358-1 2004 The platelet-derived growth factor receptor (PDGFR) is a receptor tyrosine kinase overexpressed in a subset of solid tumors and therefore is the target of drugs inhibiting this function such as imatinib mesylate (Gleevec). Imatinib Mesylate 213-220 ret proto-oncogene Homo sapiens 57-81 14666655-2 2003 We hypothesized that STI571 (Gleevec) would inhibit RET kinase and be a useful agent in the treatment of MTC. Imatinib Mesylate 21-27 ret proto-oncogene Homo sapiens 52-55 14666655-3 2003 MATERIALS AND METHODS: We determined the IC50 of STI571 for RET using an in vitro kinase assay and also examined the effects of STI571 on cellular proliferation and viability in TT cells, a human MTC cell line. Imatinib Mesylate 49-55 ret proto-oncogene Homo sapiens 60-63 14666655-7 2003 CONCLUSION: The concentrations of STI571 required to significantly inhibit RET and to inhibit TT cell proliferation are not clinically achievable. Imatinib Mesylate 34-40 ret proto-oncogene Homo sapiens 75-78 12490842-7 2002 RESULTS: RET phosphorylation was inhibited at 24 hours of exposure to 5 to 20 micromol/L STI571 and 48 hours of exposure to genistein (200 micromol/L) and allyl-geldanamycin (6 micromol/L). Imatinib Mesylate 89-95 ret proto-oncogene Homo sapiens 9-12